Endometrial hyperplasia

Endometrial hyperplasia (from Greek hyper — over, plasis — formation) is a pathological proliferative process characterized by excessive growth of the glandular component and stroma of the endometrium, leading to thickening of the mucous membrane and a shift in the gland/stroma ratio toward a predominance of glands.

Etiology and pathophysiology

The main pathogenetic driver is absolute or relative hyperestrogenism (prolonged estrogen exposure) against the background of progesterone deficiency. Estrogens stimulate mitotic activity of cells. In the absence of progesterone, which normally halts division and initiates secretory transformation, the endometrium continues to grow uncontrollably. According to the WHO classification (2014), two fundamentally different forms are distinguished:

1. Non-atypical hyperplasia: A benign process with a cancer transformation risk of less than 1-3%.
2. Atypical hyperplasia (endometrial intraepithelial neoplasia, EIN): A true precancerous condition characterized by cellular atypia (nuclear changes). Malignancy risk — 30-50%.

Clinical significance

Clinically, the condition manifests as abnormal uterine bleeding: heavy and prolonged menstruation (menorrhagia) or acyclic intermenstrual bleeding (metrorrhagia). Often associated with obesity (as adipose tissue synthesizes estrogens), polycystic ovary syndrome (owing to anovulation), and tamoxifen use. Diagnosis is confirmed histologically (following a pipelle biopsy or curettage). Atypical form requires radical treatment (often hysterectomy), especially in perimenopausal women.